Synapse loss is strongly correlated with cognitive impairment in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Synapse loss is strongly correlated with cognitive impairment in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
FE65 binds to the Alzheimer amyloid precursor protein (APP), but the function of this interaction has not been identified. 4 key findings →
Evidence: low
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Herein, we demonstrate that endogenous Tyrobp transcription is specifically increased in recruited microglia. 4 key findings →
Evidence: low
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Recent evidence suggests that high molecular weight soluble oligomeric Abeta (oAbeta) assemblies (also known as Abeta-derived diffusible ligands, or ADDLs) may represent a primary neurotoxic basis for cognitive failure in Alzheimer disease (AD). 4 key findings →
Evidence: low
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Traumatic brain injury (TBI) in early to mid-life is associated with an increased risk of dementia in late life. 4 key findings →
Participants: 62 Evidence: low
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Among 738 MA and 1488 FFS participants, weighted mean age was 76 years (SD 7.0), 59% were female, and 9% had probable dementia. 5 key findings →
Design: cohort study Evidence: moderate
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Vascular dementia (VaD) is the second leading cause of dementia after Alzheimer's disease (AD). 1 key finding →
Design: narrative review Evidence: low
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PurposeDelirium is a common yet preventable complication of hospitalization, surgery and illness that is associated with poor outcomes. 1 key finding →
Design: cohort study Evidence: moderate
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The Alzheimer's Disease Sequencing Project (ADSP) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively normal controls primarily of European ancestry (EA), among whom 218 cases and 177 controls were Caribbean Hispanic (CH). 2 key findings →
Evidence: low
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Parkinson disease (PD) and Alzheimer disease (AD), the two most common neurodegenerative disorders in American adults, are of purely genetic origin in a minority of cases and appear in most instances to arise through interactions among genetic and environmental factors. 1 key finding →
Evidence: low
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We report the neuropathological findings in 32 patients, aged 46-86 years, with dementia lacking distinctive histopathology. 4 key findings →
Participants: 32 Evidence: low
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The neural protein FE65 contains two types of protein-protein interaction modules: one WW binding domain and two phosphotyrosine binding domains. 4 key findings →
Evidence: low
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The TREM2 variant is associated with: (i) AD (odds ratio: 4.76; P = .014); (ii) increased density of amyloid plaques and neurofibrillary tangles in multiple brain regions; (iii) increased TREM2 (P = .041) and TYROBP (P = .006) gene expression; (iv) decreased TREM2 protein levels (P = .016); and (v) upregulation of proinflammatory cytokines (regulated on activation, norma 3 key findings →
Evidence: low
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Over the past decade, public awareness of the long-term pathological consequences of traumatic brain injury (TBI) has increased. 4 key findings →
Evidence: low
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Data collection began in March 2024. So far 562 people completed a pre-screening online questionnaire, with 190 passing pre-screening of whom 54% met eligibility criteria. 5 key findings →
Participants: 24 Evidence: high
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The cognitive assessment protocol of the Alzheimer's Disease Cooperative Study (ADCS) was designed to evaluate the reliability and validity of cognitive assessment measures that might be valuable additions to the Alzheimer's Disease Assessment Scale (ADAS) or other concise batteries used in antidementia drug trials.
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Clinical assessment of brain function relies heavily on indirect behavior-based tests. 1 key finding →
Evidence: low
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Oxidative stress has been proposed as a pathogenetic mechanism in Parkinson's disease (PD). 2 key findings →
Evidence: low
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Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. 4 key findings →
Evidence: low
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Overall PiB-PET uptake increased during the first two years (before ARIA-E) and decreased during the last two years (including ARIA-E episodes) (0.03±0.05 vs. -0.04±0.04 SUVR/year, p-value=0.01, Figure 2). 5 key findings →
Design: longitudinal study Evidence: moderate
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Among people with dementia, predicted 1-year mortality was higher among those with hip fracture (35.4%) versus those without hip fracture (14.8%), with similar patterns for pneumonia (49.6% vs. 13.0%). 5 key findings →
Evidence: low
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Aged individuals with Down syndrome (DS) develop senile plaques and neurofibrillary tangles consistent with Alzheimer disease (AD). 1 key finding →
Participants: 15 Evidence: low
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Before amyloid formation, peptides cleaved from the amyloid precursor protein (APP) exist as soluble oligomers. 4 key findings →
Evidence: low
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Patients with essential tremor (ET) frequently develop concurrent dementia, which is often assumed to represent co-morbid Alzheimer disease (AD). 4 key findings →
Participants: 13 Evidence: low
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Overall PiB-PET uptake increased during the first two years (before ARIA-E) and decreased during the last two years (including ARIA-E episodes) (0.03±0.05 vs. -0.04±0.04 SUVR/year, p-value=0.01, Figure 2). 5 key findings →
Design: longitudinal study Evidence: moderate
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Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,580 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.6% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →